Journal articles: 'Basal radial glia cell'

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Pereida-Jaramillo, Elizabeth, Gabriela B. Gómez-González, Angeles Edith Espino-Saldaña, and Ataúlfo Martínez-Torres. "Calcium Signaling in the Cerebellar Radial Glia and Its Association with Morphological Changes during Zebrafish Development." International Journal of Molecular Sciences 22, no. 24 (December 16, 2021): 13509. http://dx.doi.org/10.3390/ijms222413509.

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Radial glial cells are a distinct non-neuronal cell type that, during development, span the entire width of the brain walls of the ventricular system. They play a central role in the origin and placement of neurons, since their processes form structural scaffolds that guide and facilitate neuronal migration. Furthermore, glutamatergic signaling in the radial glia of the adult cerebellum (i.e., Bergmann glia), is crucial for precise motor coordination. Radial glial cells exhibit spontaneous calcium activity and functional coupling spread calcium waves. However, the origin of calcium activity in relation to the ontogeny of cerebellar radial glia has not been widely explored, and many questions remain unanswered regarding the role of radial glia in brain development in health and disease. In this study we used a combination of whole mount immunofluorescence and calcium imaging in transgenic (gfap-GCaMP6s) zebrafish to determine how development of calcium activity is related to morphological changes of the cerebellum. We found that the morphological changes in cerebellar radial glia are quite dynamic; the cells are remarkably larger and more elaborate in their soma size, process length and numbers after 7 days post fertilization. Spontaneous calcium events were scarce during the first 3 days of development and calcium waves appeared on day 5, which is associated with the onset of more complex morphologies of radial glia. Blockage of gap junction coupling inhibited the propagation of calcium waves, but not basal local calcium activity. This work establishes crucial clues in radial glia organization, morphology and calcium signaling during development and provides insight into its role in complex behavioral paradigms.

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Li, Zhen, William A. Tyler, Ella Zeldich, Gabriel Santpere Baró, Mayumi Okamoto, Tianliuyun Gao, Mingfeng Li, Nenad Sestan, and Tarik F. Haydar. "Transcriptional priming as a conserved mechanism of lineage diversification in the developing mouse and human neocortex." Science Advances 6, no. 45 (November 2020): eabd2068. http://dx.doi.org/10.1126/sciadv.abd2068.

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How the rich variety of neurons in the nervous system arises from neural stem cells is not well understood. Using single-cell RNA-sequencing and in vivo confirmation, we uncover previously unrecognized neural stem and progenitor cell diversity within the fetal mouse and human neocortex, including multiple types of radial glia and intermediate progenitors. We also observed that transcriptional priming underlies the diversification of a subset of ventricular radial glial cells in both species; genetic fate mapping confirms that the primed radial glial cells generate specific types of basal progenitors and neurons. The different precursor lineages therefore diversify streams of cell production in the developing murine and human neocortex. These data show that transcriptional priming is likely a conserved mechanism of mammalian neural precursor lineage specialization.

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Moore, Rachel, and Paula Alexandre. "Delta-Notch Signaling: The Long and The Short of a Neuron’s Influence on Progenitor Fates." Journal of Developmental Biology 8, no. 2 (March 26, 2020): 8. http://dx.doi.org/10.3390/jdb8020008.

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Maintenance of the neural progenitor pool during embryonic development is essential to promote growth of the central nervous system (CNS). The CNS is initially formed by tightly compacted proliferative neuroepithelial cells that later acquire radial glial characteristics and continue to divide at the ventricular (apical) and pial (basal) surface of the neuroepithelium to generate neurons. While neural progenitors such as neuroepithelial cells and apical radial glia form strong connections with their neighbours at the apical and basal surfaces of the neuroepithelium, neurons usually form the mantle layer at the basal surface. This review will discuss the existing evidence that supports a role for neurons, from early stages of differentiation, in promoting progenitor cell fates in the vertebrates CNS, maintaining tissue homeostasis and regulating spatiotemporal patterning of neuronal differentiation through Delta-Notch signalling.

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Kullmann, Jan A., Sophie Meyer, Fabrizia Pipicelli, Christina Kyrousi, Felix Schneider, Nora Bartels, Silvia Cappello, and Marco B. Rust. "Profilin1-Dependent F-Actin Assembly Controls Division of Apical Radial Glia and Neocortex Development." Cerebral Cortex 30, no. 6 (December 20, 2019): 3467–82. http://dx.doi.org/10.1093/cercor/bhz321.

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Abstract Neocortex development depends on neural stem cell proliferation, cell differentiation, neurogenesis, and neuronal migration. Cytoskeletal regulation is critical for all these processes, but the underlying mechanisms are only poorly understood. We previously implicated the cytoskeletal regulator profilin1 in cerebellar granule neuron migration. Since we found profilin1 expressed throughout mouse neocortex development, we here tested the hypothesis that profilin1 is crucial for neocortex development. We found no evidence for impaired neuron migration or layering in the neocortex of profilin1 mutant mice. However, proliferative activity at basal positions was doubled in the mutant neocortex during mid-neurogenesis, with a drastic and specific increase in basal Pax6+ cells indicative for elevated numbers of basal radial glia (bRG). This was accompanied by transiently increased neurogenesis and associated with mild invaginations resembling rudimentary neocortex folds. Our data are in line with a model in which profilin1-dependent actin assembly controls division of apical radial glia (aRG) and thereby the fate of their progenies. Via this mechanism, profilin1 restricts cell delamination from the ventricular surface and, hence, bRG production and thereby controls neocortex development in mice. Our data support the radial cone hypothesis” claiming that elevated bRG number causes neocortex folds.

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Penisson, Maxime, Mingyue Jin, Shengming Wang, Shinji Hirotsune, Fiona Francis, and Richard Belvindrah. "Lis1 mutation prevents basal radial glia-like cell production in the mouse." Human Molecular Genetics 31, no. 6 (October 12, 2021): 942–57. http://dx.doi.org/10.1093/hmg/ddab295.

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Abstract Human cerebral cortical malformations are associated with progenitor proliferation and neuronal migration abnormalities. Progenitor cells include apical radial glia, intermediate progenitors and basal (or outer) radial glia (bRGs or oRGs). bRGs are few in number in lissencephalic species (e.g. the mouse) but abundant in gyrencephalic brains. The LIS1 gene coding for a dynein regulator, is mutated in human lissencephaly, associated also in some cases with microcephaly. LIS1 was shown to be important during cell division and neuronal migration. Here, we generated bRG-like cells in the mouse embryonic brain, investigating the role of Lis1 in their formation. This was achieved by in utero electroporation of a hominoid-specific gene TBC1D3 (coding for a RAB-GAP protein) at mouse embryonic day (E) 14.5. We first confirmed that TBC1D3 expression in wild-type (WT) brain generates numerous Pax6+ bRG-like cells that are basally localized. Second, using the same approach, we assessed the formation of these cells in heterozygote Lis1 mutant brains. Our novel results show that Lis1 depletion in the forebrain from E9.5 prevented subsequent TBC1D3-induced bRG-like cell amplification. Indeed, we observe perturbation of the ventricular zone (VZ) in the mutant. Lis1 depletion altered adhesion proteins and mitotic spindle orientations at the ventricular surface and increased the proportion of abventricular mitoses. Progenitor outcome could not be further altered by TBC1D3. We conclude that disruption of Lis1/LIS1 dosage is likely to be detrimental for appropriate progenitor number and position, contributing to lissencephaly pathogenesis.

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Zhang, Sanguo, Huanhuan Joyce Wang, Jia Li, Xiao-Ling Hu, and Qin Shen. "Radial Glial Cell-Derived VCAM1 Regulates Cortical Angiogenesis Through Distinct Enrichments in the Proximal and Distal Radial Processes." Cerebral Cortex 30, no. 6 (January 6, 2020): 3717–30. http://dx.doi.org/10.1093/cercor/bhz337.

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Abstract Angiogenesis in the developing cerebral cortex accompanies cortical neurogenesis. However, the precise mechanisms underlying cortical angiogenesis at the embryonic stage remain largely unknown. Here, we show that radial glia-derived vascular cell adhesion molecule 1 (VCAM1) coordinates cortical vascularization through different enrichments in the proximal and distal radial glial processes. We found that VCAM1 was highly enriched around the blood vessels in the inner ventricular zone (VZ), preventing the ingrowth of blood vessels into the mitotic cell layer along the ventricular surface. Disrupting the enrichment of VCAM1 surrounding the blood vessels by a tetraspanin-blocking peptide or conditional deletion of Vcam1 gene in neural progenitor cells increased angiogenesis in the inner VZ. Conversely, VCAM1 expressed in the basal endfeet of radial glial processes promoted angiogenic sprouting from the perineural vascular plexus (PNVP). In utero, overexpression of VCAM1 increased the vessel density in the cortical plate, while knockdown of Vcam1 accomplished the opposite. In vitro, we observed that VCAM1 bidirectionally affected endothelial cell proliferation in a concentration-dependent manner. Taken together, our findings identify that distinct concentrations of VCAM1 around VZ blood vessels and the PNVP differently organize cortical angiogenesis during late embryogenesis.

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Shohayeb, Belal, Uda Ho, Yvonne Y. Yeap, Robert G. Parton, S. Sean Millard, Zhiheng Xu, Michael Piper, and Dominic C. H. Ng. "The association of microcephaly protein WDR62 with CPAP/IFT88 is required for cilia formation and neocortical development." Human Molecular Genetics 29, no. 2 (December 9, 2019): 248–63. http://dx.doi.org/10.1093/hmg/ddz281.

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Abstract WDR62 mutations that result in protein loss, truncation or single amino-acid substitutions are causative for human microcephaly, indicating critical roles in cell expansion required for brain development. WDR62 missense mutations that retain protein expression represent partial loss-of-function mutants that may therefore provide specific insights into radial glial cell processes critical for brain growth. Here we utilized CRISPR/Cas9 approaches to generate three strains of WDR62 mutant mice; WDR62 V66M/V66M and WDR62R439H/R439H mice recapitulate conserved missense mutations found in humans with microcephaly, with the third strain being a null allele (WDR62stop/stop). Each of these mutations resulted in embryonic lethality to varying degrees and gross morphological defects consistent with ciliopathies (dwarfism, anophthalmia and microcephaly). We find that WDR62 mutant proteins (V66M and R439H) localize to the basal body but fail to recruit CPAP. As a consequence, we observe deficient recruitment of IFT88, a protein that is required for cilia formation. This underpins the maintenance of radial glia as WDR62 mutations caused premature differentiation of radial glia resulting in reduced generation of neurons and cortical thinning. These findings highlight the important role of the primary cilium in neocortical expansion and implicate ciliary dysfunction as underlying the pathology of MCPH2 patients.

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Golden, J. A., J. C. Zitz, K. McFadden, and C. L. Cepko. "Cell migration in the developing chick diencephalon." Development 124, no. 18 (September 15, 1997): 3525–33. http://dx.doi.org/10.1242/dev.124.18.3525.

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We previously reported that retrovirally marked clones in the mature chick diencephalon were widely dispersed in the mediolateral, dorsoventral and rostrocaudal planes. The current study was undertaken to define the migration routes that led to the dispersion. Embryos were infected between stages 10 and 14 with a retroviral stock encoding alkaline phosphatase and a library of molecular tags. Embryos were harvested 2.5-5.5 days later and the brains were fixed and serially sectioned. Sibling relationships were determined following PCR amplification and sequencing of the molecular tag. On embryonic day 4, all clones were organized in radial columns spanning the neuroepithelium, which was composed primarily of a ventricular zone at this age. No tangential migration was seen in the ventricular zone. On embryonic day 5, most clones remained radial with many cells located in the ventricular zone; however, a few clones had cells migrating perpendicular to the radial column, in either a rostrocaudal or dorsoventral direction. The tangential migration began just beyond the basal limit of the ventricular zone. On embryonic days 6 and 7, many clones had cells migrating perpendicular to the radial column, which spanned from the ventricular to the pial surface. The migrating cells appeared to be aligned along axes that were perpendicular to the radial column. Using a combination of DiI tracing, immunohistochemistry and electron microscopy, we have determined that axonal tracts are present and are aligned with the migrating cells, suggesting that they support the non-radial cell migration. These data indicate that migration along pathways independent of radial glia occur outside of the ventricular zone in more than 50% of the clones in the chick diencephalon.

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Li, Xiaosu, Guoping Liu, Lin Yang, Zhenmeiyu Li, Zhuangzhi Zhang, Zhejun Xu, Yuqun Cai, et al. "Decoding Cortical Glial Cell Development." Neuroscience Bulletin 37, no. 4 (February 19, 2021): 440–60. http://dx.doi.org/10.1007/s12264-021-00640-9.

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AbstractMouse cortical radial glial cells (RGCs) are primary neural stem cells that give rise to cortical oligodendrocytes, astrocytes, and olfactory bulb (OB) GABAergic interneurons in late embryogenesis. There are fundamental gaps in understanding how these diverse cell subtypes are generated. Here, by combining single-cell RNA-Seq with intersectional lineage analyses, we show that beginning at around E16.5, neocortical RGCs start to generate ASCL1+EGFR+ apical multipotent intermediate progenitors (MIPCs), which then differentiate into basal MIPCs that express ASCL1, EGFR, OLIG2, and MKI67. These basal MIPCs undergo several rounds of divisions to generate most of the cortical oligodendrocytes and astrocytes and a subpopulation of OB interneurons. Finally, single-cell ATAC-Seq supported our model for the genetic logic underlying the specification and differentiation of cortical glial cells and OB interneurons. Taken together, this work reveals the process of cortical radial glial cell lineage progression and the developmental origins of cortical astrocytes and oligodendrocytes.

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Sawada, Kazuhiko. "Tracking of neurons derived from basal radial glia experiencing multiple cell division in the developing neocortex of ferrets." IBRO Reports 6 (September 2019): S84. http://dx.doi.org/10.1016/j.ibror.2019.07.272.

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Park, Seon Hye E., Ashwinikumar Kulkarni, and Genevieve Konopka. "FOXP1 orchestrates neurogenesis in human cortical basal radial glial cells." PLOS Biology 21, no. 8 (August 4, 2023): e3001852. http://dx.doi.org/10.1371/journal.pbio.3001852.

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During cortical development, human basal radial glial cells (bRGCs) are highly capable of sustained self-renewal and neurogenesis. Selective pressures on this cell type may have contributed to the evolution of the human neocortex, leading to an increase in cortical size. bRGCs have enriched expression for Forkhead Box P1 (FOXP1), a transcription factor implicated in neurodevelopmental disorders (NDDs) such as autism spectrum disorder. However, the cell type–specific roles of FOXP1 in bRGCs during cortical development remain unexplored. Here, we examine the requirement for FOXP1 gene expression regulation underlying the production of bRGCs using human brain organoids. We examine a developmental time point when FOXP1 expression is highest in the cortical progenitors, and the bRGCs, in particular, begin to actively produce neurons. With the loss of FOXP1, we show a reduction in the number of bRGCs, as well as reduced proliferation and differentiation of the remaining bRGCs, all of which lead to reduced numbers of excitatory cortical neurons over time. Using single-nuclei RNA sequencing and cell trajectory analysis, we uncover a role for FOXP1 in directing cortical progenitor proliferation and differentiation by regulating key signaling pathways related to neurogenesis and NDDs. Together, these results demonstrate that FOXP1 regulates human-specific features in early cortical development.

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Sahara, Setsuko, and Dennis D. M. O'Leary. "Fgf10 Regulates Transition Period of Cortical Stem Cell Differentiation to Radial Glia Controlling Generation of Neurons and Basal Progenitors." Neuron 63, no. 1 (July 2009): 48–62. http://dx.doi.org/10.1016/j.neuron.2009.06.006.

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Zhao, Xiang, Jason Q. Garcia, Kai Tong, Xingye Chen, Bin Yang, Qi Li, Zhipeng Dai, et al. "Polarized endosome dynamics engage cytoplasmic Par-3 that recruits dynein during asymmetric cell division." Science Advances 7, no. 24 (June 2021): eabg1244. http://dx.doi.org/10.1126/sciadv.abg1244.

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In the developing embryos, the cortical polarity regulator Par-3 is critical for establishing Notch signaling asymmetry between daughter cells during asymmetric cell division (ACD). How cortically localized Par-3 establishes asymmetric Notch activity in the nucleus is not understood. Here, using in vivo time-lapse imaging of mitotic radial glia progenitors in the developing zebrafish forebrain, we uncover that during horizontal ACD along the anteroposterior embryonic axis, endosomes containing the Notch ligand DeltaD (Dld) move toward the cleavage plane and preferentially segregate into the posterior (subsequently basal) Notchhi daughter. This asymmetric segregation requires the activity of Par-3 and dynein motor complex. Using label retention expansion microscopy, we further detect Par-3 in the cytosol colocalizing the dynein light intermediate chain 1 (Dlic1) onto Dld endosomes. Par-3, Dlic1, and Dld are associated in protein complexes in vivo. Our data reveal an unanticipated mechanism by which cytoplasmic Par-3 directly polarizes Notch signaling components during ACD.

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Stier, H., and B. Schlosshauer. "Axonal guidance in the chicken retina." Development 121, no. 5 (May 1, 1995): 1443–54. http://dx.doi.org/10.1242/dev.121.5.1443.

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During retina development, ganglion cells extend their axons exclusively into the innermost tissue layer, but not into outer retina layers. In order to elucidate guiding mechanisms for axons, tissue strips of embryonic chicken retinae were explanted onto retinal cryosections (cryoculture). Ganglion cell axons originating from the explant grew preferentially on the innermost retina layer of cryosections, whereas outer tissue layers were avoided, very much as in vivo. Stereotropism, interaction with laminin of the basal lamina and axonal fasciculation did not significantly affect oriented axonal outgrowth, so that stereotropism as a guidance mechanism could be excluded. Ganglion cell axons were not directed by physical barriers, e.g. microstructured silicon oxide chips. Similarly, UV induced protein inactivation revealed that laminin present in the inner retina did not provide a guidance cue. Even in the absence of ganglion cell axons in retinal cryosections due to prior optic nerve transection in ovo, the growth preference for the innermost retina layer was maintained in cryocultures. However, oriented elongation of axons along the innermost retina layer was lost when radial glial endfeet were selectively eliminated in retinal cryosections. In addition, glial endfeet provided an excellent growth substratum when pure preparations of endfeet were employed in explant cultures. The preference for glial endfeet positioned at the inner retina surface was accompanied by the avoidance of outer retina layers, most likely because of inhibitory components in this region. This assumption is corroborated by the finding that addition of exogenous growth-promoting laminin to cryosections did not abolish the inhibition. Laminin on glass surfaces provided an excellent substratum. Axonal outgrowth was also seriously hampered on specifically purified cells of the outer retina. Most notable, however, in cryocultures aberrant innervation of outer retina layers could be induced by prior heat or protease treatment of cryosections, which pointed to proteins as potential inhibitory components. In summary the data substantiate the hypothesis that within the retina, ganglion cell axons are guided by a dual mechanism based on a permissive and an inhibitory zone. Radial glia is likely to be instructive in this process.

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Zaidi, Donia, Kaviya Chinnappa, and Fiona Francis. "Primary Cilia Influence Progenitor Function during Cortical Development." Cells 11, no. 18 (September 16, 2022): 2895. http://dx.doi.org/10.3390/cells11182895.

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Corticogenesis is an intricate process controlled temporally and spatially by many intrinsic and extrinsic factors. Alterations during this important process can lead to severe cortical malformations. Apical neuronal progenitors are essential cells able to self-amplify and also generate basal progenitors and/or neurons. Apical radial glia (aRG) are neuronal progenitors with a unique morphology. They have a long basal process acting as a support for neuronal migration to the cortical plate and a short apical process directed towards the ventricle from which protrudes a primary cilium. This antenna-like structure allows aRG to sense cues from the embryonic cerebrospinal fluid (eCSF) helping to maintain cell shape and to influence several key functions of aRG such as proliferation and differentiation. Centrosomes, major microtubule organising centres, are crucial for cilia formation. In this review, we focus on how primary cilia influence aRG function during cortical development and pathologies which may arise due to defects in this structure. Reporting and cataloguing a number of ciliary mutant models, we discuss the importance of primary cilia for aRG function and cortical development.

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Moers, Alexandra, Alexander Nürnberg, Sandra Goebbels, Nina Wettschureck, and Stefan Offermanns. "Gα12/Gα13 Deficiency Causes Localized Overmigration of Neurons in the Developing Cerebral and Cerebellar Cortices." Molecular and Cellular Biology 28, no. 5 (December 17, 2007): 1480–88. http://dx.doi.org/10.1128/mcb.00651-07.

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ABSTRACT The heterotrimeric G proteins G12 and G13 link G-protein-coupled receptors to the regulation of the actin cytoskeleton and the induction of actomyosin-based cellular contractility. Here we show that conditional ablation of the genes encoding the α-subunits of G12 and G13 in the nervous system results in neuronal ectopia of the cerebral and cerebellar cortices due to overmigration of cortical plate neurons and cerebellar Purkinje cells, respectively. The organization of the radial glia and the basal lamina was not disturbed, and the Cajal-Retzius cell layer had formed normally in mutant mice. Embryonic cortical neurons lacking G12/G13 were unable to retract their neurites in response to lysophosphatidic acid and sphingosine-1-phosphate, indicating that they had lost the ability to respond to repulsive mediators acting via G-protein-coupled receptors. Our data indicate that G12/G13-coupled receptors mediate stop signals and are required for the proper positioning of migrating cortical plate neurons and Purkinje cells during development.

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Loeb, J. A., T. S. Khurana, J. T. Robbins, A. G. Yee, and G. D. Fischbach. "Expression patterns of transmembrane and released forms of neuregulin during spinal cord and neuromuscular synapse development." Development 126, no. 4 (February 15, 1999): 781–91. http://dx.doi.org/10.1242/dev.126.4.781.

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We mapped the distribution of neuregulin and its transmembrane precursor in developing, embryonic chick and mouse spinal cord. Neuregulin mRNA and protein were expressed in motor and sensory neurons shortly after their birth and levels steadily increased during development. Expression of the neuregulin precursor was highest in motor and sensory neuron cell bodies and axons, while soluble, released neuregulin accumulated along early motor and sensory axons, radial glia, spinal axonal tracts and neuroepithelial cells through associations with heparan sulfate proteoglycans. Neuregulin accumulation in the synaptic basal lamina of neuromuscular junctions occurred significantly later, coincident with a reorganization of muscle extracellular matrix resulting in a relative concentration of heparan sulfate proteoglycans at endplates. These results demonstrate an early axonal presence of neuregulin and its transmembrane precursor at developing synapses and a role for heparan sulfate proteoglycans in regulating the temporal and spatial sites of soluble neuregulin accumulation during development.

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D’Arcy, Brooke R., Ashley L. Lennox, Camila Manso Musso, Annalise Bracher, Carla Escobar-Tomlienovich, Stephany Perez-Sanchez, and Debra L. Silver. "Non-muscle myosins control radial glial basal endfeet to mediate interneuron organization." PLOS Biology 21, no. 2 (February 28, 2023): e3001926. http://dx.doi.org/10.1371/journal.pbio.3001926.

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Radial glial cells (RGCs) are essential for the generation and organization of neurons in the cerebral cortex. RGCs have an elongated bipolar morphology with basal and apical endfeet that reside in distinct niches. Yet, how this subcellular compartmentalization of RGCs controls cortical development is largely unknown. Here, we employ in vivo proximity labeling, in the mouse, using unfused BirA to generate the first subcellular proteome of RGCs and uncover new principles governing local control of cortical development. We discover a cohort of proteins that are significantly enriched in RGC basal endfeet, with MYH9 and MYH10 among the most abundant. Myh9 and Myh10 transcripts also localize to endfeet with distinct temporal dynamics. Although they each encode isoforms of non-muscle myosin II heavy chain, Myh9 and Myh10 have drastically different requirements for RGC integrity. Myh9 loss from RGCs decreases branching complexity and causes endfoot protrusion through the basement membrane. In contrast, Myh10 controls endfoot adhesion, as mutants have unattached apical and basal endfeet. Finally, we show that Myh9- and Myh10-mediated regulation of RGC complexity and endfoot position non-cell autonomously controls interneuron number and organization in the marginal zone. Our study demonstrates the utility of in vivo proximity labeling for dissecting local control of complex systems and reveals new mechanisms for dictating RGC integrity and cortical architecture.

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Rosenfeld, Amy B., David J. Doobin, Audrey L. Warren, Vincent R. Racaniello, and Richard B. Vallee. "Replication of early and recent Zika virus isolates throughout mouse brain development." Proceedings of the National Academy of Sciences 114, no. 46 (October 31, 2017): 12273–78. http://dx.doi.org/10.1073/pnas.1714624114.

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Fetal infection with Zika virus (ZIKV) can lead to congenital Zika virus syndrome (cZVS), which includes cortical malformations and microcephaly. The aspects of cortical development that are affected during virus infection are unknown. Using organotypic brain slice cultures generated from embryonic mice of various ages, sites of ZIKV replication including the neocortical proliferative zone and radial columns, as well as the developing midbrain, were identified. The infected radial units are surrounded by uninfected cells undergoing apoptosis, suggesting that programmed cell death may limit viral dissemination in the brain and may constrain virus-associated injury. Therefore, a critical aspect of ZIKV-induced neuropathology may be defined by death of uninfected cells. All ZIKV isolates assayed replicated efficiently in early and midgestation cultures, and two isolates examined replicated in late-gestation tissue. Alteration of neocortical cytoarchitecture, such as disruption of the highly elongated basal processes of the radial glial progenitor cells and impairment of postmitotic neuronal migration, were also observed. These data suggest that all lineages of ZIKV tested are neurotropic, and that ZIKV infection interferes with multiple aspects of neurodevelopment that contribute to the complexity of cZVS.

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Gray, J. A., G. Grigoryan, D. Virley, S. Patel, J. D. Sinden, and H. Hodges. "Conditionally Immortalized, Multipotential and Multifunctional Neural Stem Cell Lines as an Approach to Clinical Transplantation." Cell Transplantation 9, no. 2 (March 2000): 153–68. http://dx.doi.org/10.1177/096368970000900203.

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Experiments are described using rats with two kinds of brain damage and consequent cognitive deficit (in the Morris water maze, three-door runway, and radial maze): 1) ischemic damage to the CA1 hippocampal cell field after four-vessel occlusion (4VO), and 2) damage to the forebrain cholinergic projection system by local injection of excitotoxins to the nuclei of origin or prolonged ethanol administration. Cell suspension grafts derived from primary fetal brain tissue display a stringent requirement for homotypical cell replacement in the 4VO model: cells from the embryonic day (E)18–19 CA1 hippocampal subfield, but not from CA3 or dentate gyrus or from E16 basal forebrain (cholinergic rich) led to recovery of cognitive function. After damage to the cholinergic system, conversely, recovery of function was seen with cell suspension grafts from E16 basal forebrain or cholinergic-rich E14 ventral mesencephalon, but not with implants of hippocampal tissue. These two models therefore provided a test of multifunctionality for a clonal line of conditionally immortalized neural stem cells, MHP36, derived from the E14 “immortomouse” hippocampal anlage. Implanted above the damaged CA1 cell field in 4VO-treated adult rats, these cells (multipotential in vitro) migrated to the damaged area, reconstituted the gross morphology of the CA1 pyramidal layer, took up both neuronal and glial phenotypes, and gave rise to cognitive recovery. Similar recovery of function and restoration of species-typical morphology was observed when MHP36 cells were implanted into marmosets with excitotoxic CA1 damage. MHP36 implants led to recovery of cognitive function also in two experiments with rats with excitotoxic damage to the cholinergic system damage, either unilaterally in the nucleus basalis or bilaterally in both the nucleus basalis and the medial septal area. Thus, MHP36 cells are both multipotent (able to take up multiple cellular phenotypes) and multifunctional (able to repair diverse types of brain damage).

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Pushchina, Evgeniya V., Maria E. Stukaneva, and Anatoly A. Varaksin. "Hydrogen Sulfide Modulates Adult and Reparative Neurogenesis in the Cerebellum of Juvenile Masu Salmon, Oncorhynchus masou." International Journal of Molecular Sciences 21, no. 24 (December 17, 2020): 9638. http://dx.doi.org/10.3390/ijms21249638.

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Fish are a convenient model for the study of reparative and post-traumatic processes of central nervous system (CNS) recovery, because the formation of new cells in their CNS continues throughout life. After a traumatic injury to the cerebellum of juvenile masu salmon, Oncorhynchus masou, the cell composition of the neurogenic zones containing neural stem cells (NSCs)/neural progenitor cells (NPCs) in the acute period (two days post-injury) changes. The presence of neuroepithelial (NE) and radial glial (RG) neuronal precursors located in the dorsal, lateral, and basal zones of the cerebellar body was shown by the immunohistochemical (IHC) labeling of glutamine synthetase (GS). Progenitors of both types are sources of neurons in the cerebellum of juvenile O. masou during constitutive growth, thus, playing an important role in CNS homeostasis and neuronal plasticity during ontogenesis. Precursors with the RG phenotype were found in the same regions of the molecular layer as part of heterogeneous constitutive neurogenic niches. The presence of neuroepithelial and radial glia GS+ cells indicates a certain proportion of embryonic and adult progenitors and, obviously, different contributions of these cells to constitutive and reparative neurogenesis in the acute post-traumatic period. Expression of nestin and vimentin was revealed in neuroepithelial cerebellar progenitors of juvenile O. masou. Patterns of granular expression of these markers were found in neurogenic niches and adjacent areas, which probably indicates the neurotrophic and proneurogenic effects of vimentin and nestin in constitutive and post-traumatic neurogenesis and a high level of constructive metabolism. No expression of vimentin and nestin was detected in the cerebellar RG of juvenile O. masou. Thus, the molecular markers of NSCs/NPCs in the cerebellum of juvenile O. masou are as follows: vimentin, nestin, and glutamine synthetase label NE cells in intact animals and in the post-traumatic period, while GS expression is present in the RG of intact animals and decreases in the acute post-traumatic period. A study of distribution of cystathionine β-synthase (CBS) in the cerebellum of intact young O. masou showed the expression of the marker mainly in type 1 cells, corresponding to NSCs/NCPs for other molecular markers. In the post-traumatic period, the number of CBS+ cells sharply increased, which indicates the involvement of H2S in the post-traumatic response. Induction of CBS in type 3 cells indicates the involvement of H2S in the metabolism of extracellular glutamate in the cerebellum, a decrease in the production of reactive oxygen species, and also arrest of the oxidative stress development, a weakening of the toxic effects of glutamate, and a reduction in excitotoxicity. The obtained results allow us to consider H2S as a biologically active substance, the numerous known effects of which can be supplemented by participation in the processes of constitutive neurogenesis and neuronal regeneration.

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Meyerink, Brandon L., Neeraj K. Tiwari, and Louis-Jan Pilaz. "Ariadne’s Thread in the Developing Cerebral Cortex: Mechanisms Enabling the Guiding Role of the Radial Glia Basal Process during Neuron Migration." Cells 10, no. 1 (December 22, 2020): 3. http://dx.doi.org/10.3390/cells10010003.

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Radial neuron migration in the developing cerebral cortex is a complex journey, starting in the germinal zones and ending in the cortical plate. In mice, migratory distances can reach several hundreds of microns, or millimeters in humans. Along the migratory path, radially migrating neurons slither through cellularly dense and complex territories before they reach their final destination in the cortical plate. This task is facilitated by radial glia, the neural stem cells of the developing cortex. Indeed, radial glia have a unique bipolar morphology, enabling them to serve as guides for neuronal migration. The key guiding structure of radial glia is the basal process, which traverses the entire thickness of the developing cortex. Neurons recognize the basal process as their guide and maintain physical interactions with this structure until the end of migration. Thus, the radial glia basal process plays a key role during radial migration. In this review, we highlight the pathways enabling neuron-basal process interactions during migration, as well as the known mechanisms regulating the morphology of the radial glia basal process. Throughout, we describe how dysregulation of these interactions and of basal process morphology can have profound effects on cortical development, and therefore lead to neurodevelopmental diseases.

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Gray, G. E., and J. R. Sanes. "Lineage of radial glia in the chicken optic tectum." Development 114, no. 1 (January 1, 1992): 271–83. http://dx.doi.org/10.1242/dev.114.1.271.

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In many parts of the central nervous system, the elongated processes of radial glial cells are believed to guide immature neurons from the ventricular zone to their sites of differentiation. To study the clonal relationships of radial glia to other neural cell types, we used a recombinant retrovirus to label precursor cells in the chick optic tectum with a heritable marker, the E. coli lacZ gene. The progeny of the infected cells were detected at later stages of development with a histochemical stain for the lacZ gene product. Radial glia were identified in a substantial fraction of clones, and these were studied further. Our main results are the following. (a) Clones containing radial glia frequently contained neurons and/or astrocytes, but usually not other radial glia. Thus, radial glia derive from a multipotential progenitor rather than from a committed radial glial precursor. (b) Production of radial glia continues until at least embryonic day (E) 8, after the peak of neuronal birth is over (approximately E5) and after radial migration of immature neurons has begun (E6-7). Radial glial and neuronal lineages do not appear to diverge during this interval, and radial glia are among the last cells that their progenitors produce. (c) As they migrate, many cells are closely apposed to the apical process of their sibling radial glia. Thus, radial glia may frequently guide the migration of their clonal relatives. (d) The population of labelled radial glia declines between E15 and E19-20 (just before hatching), concurrent with a sharp increase in the number of labelled astrocytes. This result suggests that some tectal radial glia transform into astrocytes, as occurs in mammalian cerebral cortex, although others persist after hatching. To reconcile the observations that many radial glia are present early, that radial glia are among the last offspring of a multipotential stem cell, and that most clones contain only a single radial glial cell, we suggest that the stem cell is, or becomes, a radial glial cell.

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Kriegstein, Arnold R., and Magdalena Götz. "Radial glia diversity: A matter of cell fate." Glia 43, no. 1 (May 16, 2003): 37–43. http://dx.doi.org/10.1002/glia.10250.

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Beattie, Robert, and Simon Hippenmeyer. "Mechanisms of radial glia progenitor cell lineage progression." FEBS Letters 591, no. 24 (November 22, 2017): 3993–4008. http://dx.doi.org/10.1002/1873-3468.12906.

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Dieriks, Birger Victor, Justin M. Dean, Eleonora Aronica, Henry J. Waldvogel, Richard L. M. Faull, and Maurice A. Curtis. "Differential Fatty Acid-Binding Protein Expression in Persistent Radial Glia in the Human and Sheep Subventricular Zone." Developmental Neuroscience 40, no. 2 (2018): 145–61. http://dx.doi.org/10.1159/000487633.

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Fatty acid-binding proteins (FABPs) are a family of transport proteins that facilitate intracellular transport of fatty acids. Despite abundant expression in the brain, the role that FABPs play in the process of cell proliferation and migration in the subventricular zone (SVZ) remains unclear. Our results provide a detailed characterisation of FABP3, 5, and 7 expression in adult and fetal human and sheep SVZ. High FABP5 expression was specifically observed in the adult human SVZ and co-labelled with polysialylated neural cell adhesion molecule (PSA-NCAM), glial fibrillary acidic protein (GFAP), GFAPδ, and proliferating cell nuclear antigen (PCNA), indicating a role for FABP5 throughout the full maturation process of astrocytes and neuroblasts. Some FABP5+ cells had a radial glial-like appearance and co-labelled with the radial glia markers vimentin (40E-C) and GFAP. In the fetal human brain, FABP5 was expressed by radial glia cells throughout the ventricular zone. In contrast, radial glia-like cells in sheep highly expressed FABP3. Taken together, these differences highlight the species-specific expression profile of FABPs in the SVZ. In this study, we demonstrate the distribution of FABP in the adult human SVZ and fetal ventricular zone and reveal its expression on persistent radial glia that may be involved in adult neurogenesis.

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Matsuoka, Ryota L., Andrea Rossi, Oliver A. Stone, and Didier Y. R. Stainier. "CNS-resident progenitors direct the vascularization of neighboring tissues." Proceedings of the National Academy of Sciences 114, no. 38 (August 30, 2017): 10137–42. http://dx.doi.org/10.1073/pnas.1619300114.

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Organ growth requires the coordinated invasion and expansion of blood vessel networks directed by tissue-resident cells and morphogenetic cues. A striking example of this intercellular communication is the vascularization of the central nervous system (CNS), which is driven by neuronal progenitors, including neuroepithelial cells and radial glia. Although the importance of neuronal progenitors in vascular development within the CNS is well recognized, how these progenitors regulate the vasculature outside the CNS remains largely unknown. Here we show that CNS-resident radial glia direct the vascularization of neighboring tissues during development. We find that genetic ablation of radial glia in zebrafish larvae leads to a complete loss of the bilateral vertebral arteries (VTAs) that extend along the ventrolateral sides of the spinal cord. Importantly, VTA formation is not affected by ablation of other CNS cell types, and radial glia ablation also compromises the subsequent formation of the peri-neural vascular plexus (PNVP), a vascular network that surrounds the CNS and is critical for CNS angiogenesis. Mechanistically, we find that radial glia control these processes via Vegfab/Vegfr2 signaling:vegfabis expressed by radial glia, and genetic or pharmacological inhibition of Vegfab/Vegfr2 signaling blocks the formation of the VTAs and subsequently of the PNVP. Moreover, mosaic overexpression of Vegfab in radial glia is sufficient to partially rescue the VTA formation defect invegfabmutants. Thus, our findings identify a critical function for CNS-resident progenitors in the regulation of vascularization outside the CNS, serving as a paradigm for cross-tissue coordination of vascular morphogenesis and growth.

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Hevner, R. F., and T. F. Haydar. "The (Not Necessarily) Convoluted Role of Basal Radial Glia in Cortical Neurogenesis." Cerebral Cortex 22, no. 2 (November 23, 2011): 465–68. http://dx.doi.org/10.1093/cercor/bhr336.

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Feng, L., and N. Heintz. "Differentiating neurons activate transcription of the brain lipid-binding protein gene in radial glia through a novel regulatory element." Development 121, no. 6 (June 1, 1995): 1719–30. http://dx.doi.org/10.1242/dev.121.6.1719.

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Formation and maintenance of a radial glial scaffold is fundamental for development of the vertebrate central nervous system. In mammals, radial glia arise in the neuroepithelium immediately prior to differentiation and migration of neurons away from the ventricular zones, and they are maintained until neuronal migration subsides. We have previously shown that expression of the brain lipid-binding protein (BLBP) in radial glia throughout the developing CNS is strictly correlated with the differentiation and migration of neurons upon these cells, and that BLBP function is required to maintain differentiation of primary cerebellar glial cells in vitro (Feng, L., Hatten, M. E. and Heintz, N. (1994). Neuron 12, 895–908). In this study, we demonstrate that BLBP transcription in vivo involves multiple regulatory elements, and that the dynamic temporal and spatial pattern of BLBP expression in radial and Bergmann glial cells throughout the developing CNS is programmed by a single radial glial cell-specific element (RGE). Furthermore, we demonstrate that BLBP expression in primary cerebellar glial cells requires coculture with differentiating neurons, and that this induction is regulated by the radial glia-specific element. The fact that transcription of BLBP in response to neurons in vitro and its dynamic regulation in radial glia throughout the CNS in vivo are both controlled by the RGE provides the first direct evidence supporting a role for differentiating neurons in the epigenetic regulation of radial glial cell function in vivo.

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Malatesta, P., and M. Gotz. "Radial glia - from boring cables to stem cell stars." Development 140, no. 3 (January 4, 2013): 483–86. http://dx.doi.org/10.1242/dev.085852.

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Nagashima, Mikiko, and Peter F. Hitchcock. "Inflammation Regulates the Multi-Step Process of Retinal Regeneration in Zebrafish." Cells 10, no. 4 (April 1, 2021): 783. http://dx.doi.org/10.3390/cells10040783.

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The ability to regenerate tissues varies between species and between tissues within a species. Mammals have a limited ability to regenerate tissues, whereas zebrafish possess the ability to regenerate almost all tissues and organs, including fin, heart, kidney, brain, and retina. In the zebrafish brain, injury and cell death activate complex signaling networks that stimulate radial glia to reprogram into neural stem-like cells that repair the injury. In the retina, a popular model for investigating neuronal regeneration, Müller glia, radial glia unique to the retina, reprogram into stem-like cells and undergo a single asymmetric division to generate multi-potent retinal progenitors. Müller glia-derived progenitors then divide rapidly, numerically matching the magnitude of the cell death, and differentiate into the ablated neurons. Emerging evidence reveals that inflammation plays an essential role in this multi-step process of retinal regeneration. This review summarizes the current knowledge of the inflammatory events during retinal regeneration and highlights the mechanisms whereby inflammatory molecules regulate the quiescence and division of Müller glia, the proliferation of Müller glia-derived progenitors and the survival of regenerated neurons.

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Kanatani, Shigeaki, Hidenori Tabata, and Kazunori Nakajima. "Topical Review: Neuronal Migration in Cortical Development." Journal of Child Neurology 19, no. 3 (March 2004): 274–79. http://dx.doi.org/10.1177/08830738040190030201.

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Cortical formation in the developing brain is a highly complicated process involving neuronal production (through symmetric or asymmetric cell division) interaction of radial glia with neuronal migration, and multiple modes of neuronal migration. It has been convincingly demonstrated by numerous studies that radial glial cells are neural stem cells. However, the processes by which neurons arise from radial glia and migrate to their final destinations in vivo are not yet fully understood. Recent studies using time-lapse imaging of neuronal migration are giving investigators an increasingly more detailed understanding of the mitotic behavior of radial glia and the migrating behavior of their daughter cells. In this review, we describe recent progress in elucidating neuronal migration in brain formation and how neuronal migration is disturbed by mutations in genes that control this process. ( J Child Neurol 2005;20:274—279).

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Nodari, Alessandro, Desirée Zambroni, Angelo Quattrini, Felipe A. Court, Alessandra D'Urso, Alessandra Recchia, Victor L. J. Tybulewicz, Lawrence Wrabetz, and M. Laura Feltri. "β1 integrin activates Rac1 in Schwann cells to generate radial lamellae during axonal sorting and myelination." Journal of Cell Biology 177, no. 6 (June 18, 2007): 1063–75. http://dx.doi.org/10.1083/jcb.200610014.

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Myelin is a multispiraled extension of glial membrane that surrounds axons. How glia extend a surface many-fold larger than their body is poorly understood. Schwann cells are peripheral glia and insert radial cytoplasmic extensions into bundles of axons to sort, ensheath, and myelinate them. Laminins and β1 integrins are required for axonal sorting, but the downstream signals are largely unknown. We show that Schwann cells devoid of β1 integrin migrate to and elongate on axons but cannot extend radial lamellae of cytoplasm, similar to cells with low Rac1 activation. Accordingly, active Rac1 is decreased in β1 integrin–null nerves, inhibiting Rac1 activity decreases radial lamellae in Schwann cells, and ablating Rac1 in Schwann cells of transgenic mice delays axonal sorting and impairs myelination. Finally, expressing active Rac1 in β1 integrin–null nerves improves sorting. Thus, increased activation of Rac1 by β1 integrins allows Schwann cells to switch from migration/elongation to the extension of radial membranes required for axonal sorting and myelination.

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Kyrousi, Christina, Zoi Lygerou, and Stavros Taraviras. "How a radial glial cell decides to become a multiciliated ependymal cell." Glia 65, no. 7 (February 7, 2017): 1032–42. http://dx.doi.org/10.1002/glia.23118.

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Kriho, V., H. Y. Yang, C. M. Lue, N. Lieska, and G. D. Pappas. "An Early Developmental Marker for Radial Glia in Rat Spinal Cord." Proceedings, annual meeting, Electron Microscopy Society of America 54 (August 11, 1996): 36–37. http://dx.doi.org/10.1017/s0424820100162648.

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Radial glia have been classically defined as those early glial cells that radially span their thin processes from the ventricular to the pial surfaces in the developing central nervous system. These radial glia constitute a transient cell population, disappearing, for the most part, by the end of the period of neuronal migration. Traditionally, it has been difficult to definitively identify these cells because the principal criteria available were morphologic only.Using immunofluorescence microscopy, we have previously defined a phenotype for radial glia in rat spinal cord based upon the sequential expression of vimentin, glial fibrillary acidic protein and an intermediate filament-associated protein, IFAP-70/280kD. We report here the application of another intermediate filament-associated protein, IFAP-300kD, originally identified in BHK-21 cells, to the immunofluorescence study of radial glia in the developing rat spinal cord.Results showed that IFAP-300kD appeared very early in rat spinal cord development. In fact by embryonic day 13, IFAP-300kD immunoreactivity was already at its peak and was observed in most of the radial glia which span the spinal cord from the ventricular to the subpial surfaces (Fig. 1). Interestingly, from this time, IFAP-300kD immunoreactivity diminished rapidly in a dorsal to ventral manner, so that by embryonic day 16 it was detectable only in the maturing macroglial cells in the marginal zone of the spinal cord and the dorsal median septum (Fig. 2). By birth, the spinal cord was essentially immuno-negative for this IFAP. Thus, IFAP-300kD appears to be another differentiation marker available for future studies of gliogenesis, especially for the early stages of radial glia differentiation.

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Wong, Fong Kuan, Ji-Feng Fei, Felipe Mora-Bermúdez, Elena Taverna, Christiane Haffner, Jun Fu, Konstantinos Anastassiadis, A. Francis Stewart, and Wieland B. Huttner. "Sustained Pax6 Expression Generates Primate-like Basal Radial Glia in Developing Mouse Neocortex." PLOS Biology 13, no. 8 (August 7, 2015): e1002217. http://dx.doi.org/10.1371/journal.pbio.1002217.

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Berg, Daniel A., Allison M. Bond, Guo-li Ming, and Hongjun Song. "Radial glial cells in the adult dentate gyrus: what are they and where do they come from?" F1000Research 7 (March 5, 2018): 277. http://dx.doi.org/10.12688/f1000research.12684.1.

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Adult neurogenesis occurs in the dentate gyrus in the mammalian hippocampus. These new neurons arise from neural precursor cells named radial glia-like cells, which are situated in the subgranular zone of the dentate gyrus. Here, we review the emerging topic of precursor heterogeneity in the adult subgranular zone. We also discuss how this heterogeneity may be established during development and focus on the embryonic origin of the dentate gyrus and radial glia-like stem cells. Finally, we discuss recently developed single-cell techniques, which we believe will be critical to comprehensively investigate adult neural stem cell origin and heterogeneity.

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Wang, Rong, Roshan Sharma, Xiaojuan Shen, Ashley M. Laughney, Kosuke Funato, Philip J. Clark, Monika Shpokayte, et al. "Adult Human Glioblastomas Harbor Radial Glia-like Cells." Stem Cell Reports 15, no. 1 (July 2020): 275–77. http://dx.doi.org/10.1016/j.stemcr.2020.06.002.

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Wang, Rong, Roshan Sharma, Xiaojuan Shen, Ashley M. Laughney, Kosuke Funato, Philip J. Clark, Monika Shpokayte, et al. "Adult Human Glioblastomas Harbor Radial Glia-like Cells." Stem Cell Reports 14, no. 2 (February 2020): 338–50. http://dx.doi.org/10.1016/j.stemcr.2020.01.007.

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Hartfuss, Eva, Rossella Galli, Nico Heins, and Magdalena Götz. "Characterization of CNS Precursor Subtypes and Radial Glia." Developmental Biology 229, no. 1 (January 2001): 15–30. http://dx.doi.org/10.1006/dbio.2000.9962.

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Liour, Sean S., Stacey A. Kraemer, Michael B. Dinkins, Chen-Ying Su, Makoto Yanagisawa, and Robert K. Yu. "Further characterization of embryonic stem cell-derived radial glial cells." Glia 53, no. 1 (January 1, 2006): 43–56. http://dx.doi.org/10.1002/glia.20257.

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Gao, Xue-Ling, Wen-Jia Tian, Bofeng Liu, Jingyi Wu, Wei Xie, and Qin Shen. "High-mobility group nucleosomal binding domain 2 protects against microcephaly by maintaining global chromatin accessibility during corticogenesis." Journal of Biological Chemistry 295, no. 2 (November 7, 2019): 468–80. http://dx.doi.org/10.1074/jbc.ra119.010616.

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The surface area of the human cerebral cortex undergoes dramatic expansion during late fetal development, leading to cortical folding, an evolutionary feature not present in rodents. Microcephaly is a neurodevelopmental disorder defined by an abnormally small brain, and many gene mutations have been found to be associated with primary microcephaly. However, mouse models generated by ablating primary microcephaly-associated genes often fail to recapitulate the severe loss of cortical surface area observed in individuals with this pathology. Here, we show that a mouse model with deficient expression of high-mobility group nucleosomal binding domain 2 (HMGN2) manifests microcephaly with reduced cortical surface area and almost normal radial corticogenesis, with a pattern of incomplete penetrance. We revealed that altered cleavage plane and mitotic delay of ventricular radial glia may explain the rising ratio of intermediate progenitor cells to radial glia and the displacement of neural progenitor cells in microcephalic mutant mice. These led to decreased self-renewal of the radial glia and reduction in lateral expansion. Furthermore, we found that HMGN2 protected corticogenesis by maintaining global chromatin accessibility mainly at promoter regions, thereby ensuring the correct regulation of the transcriptome. Our findings underscore the importance of the regulation of chromatin structure in cortical development and highlight a mouse model with critical insights into the etiology of microcephaly.

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Taylor, Michael D., Helen Poppleton, Christine Fuller, Xiaoping Su, Yongxing Liu, Patricia Jensen, Susan Magdaleno, et al. "Radial glia cells are candidate stem cells of ependymoma." Cancer Cell 8, no. 4 (October 2005): 323–35. http://dx.doi.org/10.1016/j.ccr.2005.09.001.

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Taylor, Michael D., Helen Poppleton, Christine Fuller, Xiaoping Su, Yongxing Liu, Patricia Jensen, Susan Magdaleno, et al. "Radial glia cells are candidate stem cells of ependymoma." Cancer Cell 9, no. 1 (January 2006): 70. http://dx.doi.org/10.1016/j.ccr.2005.12.023.

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Bilinovich, Stephanie M., Katie L. Uhl, Kristy Lewis, Xavier Soehnlen, Michael Williams, Daniel Vogt, Jeremy W. Prokop, and Daniel B. Campbell. "Integrated RNA Sequencing Reveals Epigenetic Impacts of Diesel Particulate Matter Exposure in Human Cerebral Organoids." Developmental Neuroscience 42, no. 5-6 (2020): 195–207. http://dx.doi.org/10.1159/000513536.

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Autism spectrum disorder (ASD) manifests early in childhood. While genetic variants increase risk for ASD, a growing body of literature has established that in utero chemical exposures also contribute to ASD risk. These chemicals include air-based pollutants like diesel particulate matter (DPM). A combination of single-cell and direct transcriptomics of DPM-exposed human-induced pluripotent stem cell-derived cerebral organoids revealed toxicogenomic effects of DPM exposure during fetal brain development. Direct transcriptomics, sequencing RNA bases via Nanopore, revealed that cerebral organoids contain extensive RNA modifications, with DPM-altering cytosine methylation in oxidative mitochondrial transcripts expressed in outer radial glia cells. Single-cell transcriptomics further confirmed an oxidative phosphorylation change in cell groups such as outer radial glia upon DPM exposure. This approach highlights how DPM exposure perturbs normal mitochondrial function and cellular respiration during early brain development, which may contribute to developmental disorders like ASD by altering neurodevelopment.

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Shtaya, Anan, Ahmed‐Ramadan Sadek, Malik Zaben, Gerald Seifert, Ashley Pringle, Christian Steinhäuser, and William Peter Gray. "AMPA receptors and seizures mediate hippocampal radial glia‐like stem cell proliferation." Glia 66, no. 11 (October 25, 2018): 2397–413. http://dx.doi.org/10.1002/glia.23479.

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Eze, Ugomma C., Aparna Bhaduri, Maximilian Haeussler, Tomasz J. Nowakowski, and Arnold R. Kriegstein. "Single-cell atlas of early human brain development highlights heterogeneity of human neuroepithelial cells and early radial glia." Nature Neuroscience 24, no. 4 (March 15, 2021): 584–94. http://dx.doi.org/10.1038/s41593-020-00794-1.

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AbstractThe human cortex comprises diverse cell types that emerge from an initially uniform neuroepithelium that gives rise to radial glia, the neural stem cells of the cortex. To characterize the earliest stages of human brain development, we performed single-cell RNA-sequencing across regions of the developing human brain, including the telencephalon, diencephalon, midbrain, hindbrain and cerebellum. We identify nine progenitor populations physically proximal to the telencephalon, suggesting more heterogeneity than previously described, including a highly prevalent mesenchymal-like population that disappears once neurogenesis begins. Comparison of human and mouse progenitor populations at corresponding stages identifies two progenitor clusters that are enriched in the early stages of human cortical development. We also find that organoid systems display low fidelity to neuroepithelial and early radial glia cell types, but improve as neurogenesis progresses. Overall, we provide a comprehensive molecular and spatial atlas of early stages of human brain and cortical development.

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Zou, Jian, Ryan P. Vetreno, and Fulton T. Crews. "ATP-P2X7 receptor signaling controls basal and TNFα-stimulated glial cell proliferation." Glia 60, no. 4 (February 1, 2012): 661–73. http://dx.doi.org/10.1002/glia.22302.

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Raphael, Alya R., David A. Lyons, and William S. Talbot. "ErbB signaling has a role in radial sorting independent of Schwann cell number." Glia 59, no. 7 (April 12, 2011): 1047–55. http://dx.doi.org/10.1002/glia.21175.

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Vaid, Samir, J. Gray Camp, Lena Hersemann, Christina Eugster Oegema, Anne-Kristin Heninger, Sylke Winkler, Holger Brandl, et al. "A novel population of Hopx-dependent basal radial glial cells in the developing mouse neocortex." Development 145, no. 20 (September 28, 2018): dev169276. http://dx.doi.org/10.1242/dev.169276.

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Journal articles on the topic 'Basal radial glia cell'

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